Renal Pharmacology Objectives Flashcards
- List the three most common organ systems whose failure results in edema formation in veterinary patients.
Congestive heart failure
Hepatic disease
Renal disease
- Describe limitations on how EPO must be administered in order to be effective.
Administer with iron supplementation to prevent iron deficiency
Injectable (SQ) only
- Describe potential adverse reactions associated with EPO use and how these might be avoided.
Iron deficiency - monitor serum iron and TIBC; administer with iron supplement
Hypertension +/- hyperviscosity if doses too high or frequent
Development of autoantibodies with resultant resistance to further treatment - Darbepoetin may be less antigenic
- Describe the rationale for the proposed use of erythropoietin (EPO) in renal failure as well as its mechanism of action.
Patients with chronic renal failure have low EPO levels which results in normocytic, normochromic nonregenerative anemia.
MOA: EPO is normally produced by peritubular fibroblasts of the renal cortex in response to low oxygenation. Erythropoietin acts on the bone marrow to increase production of RBCs but also enhances RBC survival.
- List contraindications to the use of calcitriol as well as potential adverse effects.
DO NOT USE in patients with serum phosphorous concentrations above 6.0 mg/dL (serum calcium x P product > 70 is likely to promote soft tissue mineralization).
- Describe the rationale for the proposed use of calcitriol in renal failure as well as its mechanism of action.
Because calcitriol normally inhibits synthesis of PTH, low levels of calcitriol result in elevated PTH levels—thus, supplementing calcitriol lowers the pathologic elevation in PTH in patients with chronic renal failure.
MOA: Calcitriol, 1,25 dihydroxycholecalciferol, is the biologically active form of vitamin D. The liver 25-hydroxylation is much less controlled than the highly regulated 1-alpha hydroxylation of 25- hydroxyvitamin D that takes place almost exclusively in proximal tubule cells of the kidney.
- Describe the general secondary effects of diuretic therapy (i.e., on electrolytes and renal hemodynamics).
Altering elimination of other ions including K+, H+, Ca++, Mg++, Cl-, HCO3-, and phosphates
Altering renal hemodynamics (decreased renal blood flow).
- Explain the goal of diuretic therapy as well as how that goal is accomplished.
Primary goal is to increase excretion of water - generally accomplished by increasing Na excretion.
- Provide examples of drug interactions that arise from competition for OATS and OCTS.
- Describe the function of the various renal epithelial anion and cation transporters with regard to both endogenous substrates as well as exogenous substrates (pharmacological agents).
Specialized transporters are present along the nephron.
Many drugs rely on these transporters to gain access to renal tubules.
